Summary
Light and electron microscopic morphometry was carried out in tissue samples which were obtained from the left ventricular free wall in 29 patients with chronic aortic valve disease during open-heart surgery. 6 patients had aortic stenosis, 9 had aortic insufficiency and 14 had a mixed aortic valve lesson. Hemodynamics were studied before operation. Patients with mixed aortic valve disease had a higher left ventricular mass, a lower ejection fraction and mean circumferential fiber shortening rate than patients with aortic stenosis. Peak systolic wall stress was comparable between groups. The intracellular content of contractile material was lower and the sarcoplasmic volume was higher in mixed aortic valve disease than in aortic stenosis. Mitochondrial volume and interstitial fibrosis were not different between groups. Patients with aortic insufficiency showed no significant difference of parameters as compared to both other groups. We conclude that an intracellular deficiency of myofibrils causes lack of contractility in advanced hypertrophy due to mixed aortic valve disease.
Zusammenfassung
Licht- und elektronenoptische Morphometrie wurde an Gewebeproben des linken Ventrikels durchgeführt, die bei der Herzoperation entnommen wurden. 6 Patienten hatten eine Aortenstenose, 9 eine Aorteininsuffizienz und 14 ein kombiniertes Aortenvitium. Hämodynamische Messungen wurden vor der Operation durchgeführt. Patienten mit kombiniertem Aortenvitium hatten eine höhere linksventrikuläre Masse, eine niedrigere Ejektionsfraktion und Verkürzungsgeschwindigkeit als Patienten mit Aortenstenose. Der systolische “Wall Stress” war vergleichbar in den 3 Gruppen. Der intrazelluläre Gehalt an Myofibrillen war geringer, und der sarkoplasmatische Raum war höher bei kombinierten Aortenvitien als bei Aortenstenose. Das Mitochondrienvolumen und die interstitielle Fibrose waren nicht unterschiedlich in den Gruppen. Patienten mit Aorteninsuffizienz zeigten keinen signifikanten Unterschied zu den beiden anderen Gruppen. Wir schließen daraus, daß eine intrazelluläre Verarmung von kontraktilem Material die Ursache der eingeschränkten Myokardfunktion bei fortgeschrittener Hypertrophie infolge kombinierten Aortenvitiums ist.
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Paper, presented at the Erwin Riesch Symposium, Tübingen, April 3–7, 1979
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Schwarz, F., Kittstein, D., Winkler, B. et al. Quantitative ultrastructure of the myocardium in chronic aortic valve disease. Basic Res Cardiol 75, 109–117 (1980). https://doi.org/10.1007/BF02001402
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DOI: https://doi.org/10.1007/BF02001402